For example, claudin-1 and claudin-2 modulate anoikis to induce cancer progression in a Src-Akt-Bcl-2- and epithelial growth factor receptor (EGFR)-dependent manner, respectively, while loss of claudin-18.1 increases anchorage-independent colony formation in vitro in lung cancer cells through activation of YAP/TAZ, insulin-like growth factor receptor-1 (IGF-1R) and AKT signaling (35, 36, 101, 102). This evidence concerns the gene IGF1R and lung cancer.